ライフサイエンスコーパス: IRF-1

1 IRF-1 contributed significantly to I/R injury because IR

2 IRF-1 deficiency in liver grafts, but not in recipients,

3 IRF-1 expression limited CHIKV-induced foot swelling in

4 IRF-1 induction results in cleavage of caspase-8, -3 and

5 IRF-1 is a tumor suppressor protein that activates gene

6 IRF-1 mRNA up-regulation was typically seen in graft hep

7 IRF-1 restricts the replication of diverse viruses; howe

8 IRF-1 transcriptional activity in MCF-7/LCC9 cells is 18

9 IRF-1 was induced in liver grafts immediately after repe

10 IRF-1(-/-) BMMs demonstrated enhanced LPS-induced Il23a

11 IRF-1-induced apoptosis involves caspase-8 since apoptos

12 IRF-1-KO livers had significantly reduced NK, NKT, and C

13 egulation of interferon regulatory factor 1 (IRF-1) and decreased levels of Stat1.

14 ption factor interferon regulatory factor 1 (IRF-1) and expression of microRNA 126 (miR-126).

15 slocation of interferon regulatory factor 1 (IRF-1) and IRF-8.

16 ways, one involving IFN regulatory factor 1 (IRF-1) and the other nuclear factor-kappaB (NF-kappaB).

17 tion factors interferon regulatory factor 1 (IRF-1) and upstream stimulatory factor 1 (USF-1) in gamm

18 ignaling and interferon regulatory factor 1 (IRF-1) expression is required to ensure survival of a ga

19 phism in the interferon regulatory factor 1 (IRF-1) gene has previously been reported, implicating IR

20 ption factor interferon regulatory factor 1 (IRF-1) has a demonstrated role in shaping innate and ada

21 ranscription factor IFN regulatory factor 1 (IRF-1) in mouse liver was dramatically upregulated by al

22 Interferon regulatory factor 1 (IRF-1) is a transcription factor that has been implicate

23 Interferon regulatory factor 1 (IRF-1) is a transcription factor that regulates innate a

24 g.IMPORTANCE Interferon regulatory factor 1 (IRF-1) is a transcription factor that regulates the expr

25 Interferon regulatory factor 1 (IRF-1) is a tumor suppressor that is also involved in th

26 Interferon (IFN) regulatory factor 1 (IRF-1) is a tumor suppressor that is also involved in th

27 Interferon regulatory factor 1 (IRF-1) is an important transcription factor in interfero

28 ption factor interferon regulatory factor 1 (IRF-1) is required for control of murine NV (MNV) replic

29 -suppressive interferon regulatory factor 1 (IRF-1) selectively promotes the murine gammaherpesvirus

30 y identifies interferon-regulatory factor 1 (IRF-1) to be one of such candidate host factors.

31 gnaling, and interferon regulatory factor 1 (IRF-1) transactivation.

32 Here, we found that IFN regulatory factor 1 (IRF-1) was a critical, early proinflammatory signal rele

33 roreceptor to endow IFN regulatory factor 1 (IRF-1) with apoptotic functions, which redirect murine n

34 ocyte expression of IFN regulatory factor 1 (IRF-1), a key transcription factor that regulates apopto

35 e absence of interferon-regulatory factor 1 (IRF-1), a transcription factor with antiviral and tumor

36 xpression of interferon regulatory factor 1 (IRF-1), which is important for IFN-gamma-induced C4 expr

37 , especially interferon regulatory factor-1 (IRF-1) and interferon regulatory factor-8 (IRF-8 or ICSB

38 egulation of Interferon Regulatory Factor-1 (IRF-1) and IRF-8.

39 IFN regulatory factor-1 (IRF-1) is a nuclear transcription factor that plays a cr

40 Interferon regulatory factor-1 (IRF-1) is a transcription factor and tumor suppressor th

41 Interferon (IFN) regulatory factor-1 (IRF-1) is a transcription factor that has apoptotic anti

42 Interferon regulatory factor-1 (IRF-1) is a transcription factor that regulates gene exp

43 Interferon regulatory factor-1 (IRF-1) is a transcriptional regulator that promotes apop

44 gulating the interferon regulatory factor-1 (IRF-1) tumor suppressor protein is limited.

45 in DCs deficient in IFN regulatory factor-1 (IRF-1), a key transcription factor required for IL-12 pr

46 ing site for interferon regulatory factor-1 (IRF-1), a major interferon-induced transcription factor.

47 duced expression of IFN regulatory factor-1 (IRF-1), an important transcription factor involved in ce

48 tion gene 2 (BTG2), IFN regulatory factor-1 (IRF-1), and the chemokine Gro-beta.

49 le genes, including IFN regulatory factor-1 (IRF-1), was significantly reduced in trophoblast cells c

50 tudy illustrates the crucial roles for AP-1, IRF-1, IRF-2, and STAT1 in the regulation of murine TLR9

51 y by trinitrobenzenesulfonic acid, and IL-10/IRF-1 double-deficient (IL-10/IRF-1(-/-)) mice demonstra

52 ated levels of Il23a were increased in IL-10/IRF-1(-/-) compared with WT and IL-10(-/-) colonic CD11b

53 cid, and IL-10/IRF-1 double-deficient (IL-10/IRF-1(-/-)) mice demonstrated more severe colonic inflam

54 The miR-31/IRF-1/CTSS pathway may play a functional role in the pat

55 pid Tam signaling transcriptionally activate IRF-1 through recruitment of CBP to the IRF-1 GAS promot

56 induces an autocrine pathway that activates IRF-1 and IRF-8, ultimately resulting in IL-12 transcrip

57 t of tumor-bearing mice with intratumoral Ad-IRF-1 injections results in tumor growth inhibition.

58 is observed in tumor cells infected with Ad-IRF-1 compared with Ad-Psi5 mock-infected cells and that

59 cancer cell line MDA-MB-468 infected with Ad-IRF-1, we observed a 15-fold down-regulation of the surv

60 ibroblasts, using Western immunoblot with an IRF-1-specific antiserum, to examine possible difference

61 mma in a manner dependent only on STAT-1 and IRF-1.

62 sducer and activator of transcription-1, and IRF-1 and that an RARalpha antagonist was able to inhibi

63 finding by documenting binding of GATA-4 and IRF-1 and IRF-2 to the first intron sequence.

64 n (UW) solution in wildtype (WT) C57BL/6 and IRF-1 knockout (KO) mice.

65 bservation, overexpression of both IRF-8 and IRF-1 additively activated IL-27 p28 promoter.

66 GF-beta signaling, NF-kappaB activation, and IRF-1 transactivation pathways.

67 translocation of both PKC(alpha/betaII) and IRF-1 that subsequently inhibits CIITA expression.

68 binding sequences within Gro-beta, BTG2, and IRF-1 promoters showed that MIS stimulated binding of p5

69 Control and IRF-1 small interfering RNA (siRNA) were used to analyze

70 ays of TNFalpha-induced IRF-1 expression and IRF-1 nuclear translocation.

71 amma is mediated by IRF-1 and IFN-gamma, and IRF-1-induced apoptosis is caspase-mediated.

72 fine the c-REL/p65 NF-kappaB heterodimer and IRF-1 as key transcriptional activators and ZEB1, B lymp

73 re, we show that type I interferon (IFN) and IRF-1 cooperate to control acute gammaherpesvirus infect

74 However, the role of IFNgamma and IRF-1 in the regulation of RANTES gene expression and th

75 d transcription via activating NF-kappaB and IRF-1, to induce pro-inflammatory cytokines.

76 cytes these IFN-independent require MAVS and IRF-1.

77 Specifically, both type I IFN receptor and IRF-1 expression potentiated antiviral effects of type I

78 divergent effects on TGF-beta signaling and IRF-1 transactivation.

79 eluted and analyzed by immunoblot with anti-IRF-1.

80 Basal IRF-1 mRNA expression is lower in MCF7/LCC9 cells when c

81 tributed significantly to I/R injury because IRF-1-knockout (KO) grafts displayed much less damage as

82 dies reveal an intriguing cross talk between IRF-1 and type I and II IFNs in the induction of the ant

83 On the basis of its biology, IRF-1 represents a plausible host factor to attenuate ga

84 showed that 16-kDa PRL specifically blocked IRF-1 but not NF-kappaB signaling to the iNOS promoter.

85 t a role for the Mf1 domain in limiting both IRF-1-dependent transcription and the rate of IRF-1 turn

86 , IRF-7 expression was detected by 12 h, but IRF-1 expression was not detected until 24 h after infec

87 ed antiviral responses, IFN-independent, but IRF-1- and IRF-5-dependent mechanisms, restrict HCV repl

88 cells, apoptosis by IFN-gamma is mediated by IRF-1 and IFN-gamma, and IRF-1-induced apoptosis is casp

89 ced pathway in RANTES expression mediated by IRF-1 in macrophages and elucidates an important host de

90 and death receptor 5, which are regulated by IRF-1.

91 ntrinsic, we generated mice with conditional IRF-1 deficiency.

92 Consequently, IRF-1(-/-) mice were more susceptible to colonic injury

93 In the cytoplasm, IRF-1 can no longer serve as an anti-viral transcription

94 accumulation of nuclear but not cytoplasmic IRF-1.

95 Decreased IRF-1 mRNA expression in trophoblast cells was due to a

96 ched in nonesterified fatty acids, decreased IRF-1 expression, increased miR-126 activity, and dimini

97 Additionally, we found decreased IRF-1 expression in cases of human posttransplant lympho

98 Further, we found decreased IRF-1 expression in human gammaherpesvirus-induced B cel

99 ithelial cells with a miR-31 mimic decreased IRF-1 protein levels with concomitant knockdown of CTSS

100 in interferon regulatory factor 1-deficient (IRF-1(-/-)) mice, suggesting that these islands do not c

101 in interferon regulatory factor 1-deficient (IRF-1(-/-)) mice; however, only the GR019 (virB4) mutant

102 2alpha phosphorylation, IkappaB degradation, IRF-1 expression, and STAT1 phosphorylation, resulting i

103 ecipitation analyses using the DPE-dependent IRF-1 and TAF7 promoters demonstrated that CK2, and PC4

104 ver, it appeared that the hepatocyte-derived IRF-1 was mainly responsible for alpha-GalCer-induced li

105 Irf-1 mRNA expression, but rather diminished IRF-1 protein levels and nuclear localization.

106 was higher when siRNA was used to knock down IRF-1 expression.

107 Using siRNA to knock down IRF-1, we observed reduced IL-18BPa expression.

108 expression of STAT1, or its target effector IRF-1, rescued multiple defects in Gata1-deficient megak

109 uced STAT6 phosphorylation serves to enhance IRF-1 transcription and promotes its egress from the nuc

110 layers of the retina constitutively express IRF-1 and IRF-8 and enhanced CFH expression in the retin

111 hat both NKT cells and hepatocytes expressed IRF-1 in response to alpha-GalCer.

112 thermore, levels of the transcription factor IRF-1 correlated with increased levels of its target gen

113 The host transcription factor IRF-1, a well-established tumor suppressor, selectively

114 (encoding PD-L1) by the transcription factor IRF-1, which induced the acetylation of Histone H3 at CD

115 ng TNF induction of the transcription factor IRF-1.

116 ing domains of interferon regulatory factors IRF-1 (DBD1) and IRF-3 (DBD3) were studied using microca

117 s are mediated by two transcription factors, IRF-1 (interferon-regulatory factor-1) and ICSBP (interf

118 rotein interactions; however, relatively few IRF-1-interacting proteins have been described.

119 f our study define an unappreciated role for IRF-1 in B cell biology and provide insight into the pot

120 udies documenting a cell-autonomous role for IRF-1 in gamma interferon (IFN-gamma)-mediated inhibitio

121 These studies identify a key role for IRF-1 in IFN-gamma-dependent control of norovirus infect

122 The study identifies a critical role for IRF-1 in liver transplant I/R injury.

123 binding gave an increase in expression from IRF-1-responsive promoters of up to 8-fold.

124 Functionally, IRF-1 is a negative regulator of Il23a in LPS-stimulated

125 tion and activation of the Stat1 target gene IRF-1.

126 tivated downstream signal (STAT1) and genes (IRF-1, p21(cip1), and SOCS1) in liver regeneration and h

127 unveiled in MHV68-infected mice with global IRF-1 deficiency are mediated via IRF-1 expression by no

128 Notably, hepatic IRF-1 expression was reduced significantly by neutralizi

129 r pDC to induce liver damage through hepatic IRF-1 up-regulation after I/R injury.

130 ts showed that grafts lacking hepatocellular IRF-1 had better protection compared with those lacking

131 as a consequence of induction of hepatocyte IRF-1 expression.

132 However, IRF-1 was required for optimal expression of cholesterol

133 the level of TLR9 induction was decreased in IRF-1-/- cells.

134 on cell proliferation was also diminished in IRF-1(-/-) and p21(cip1-/-) hepatocytes, but enhanced in

135 I:C on liver regeneration was diminished in IRF-1(-/-) and p21(cip1-/-)mice.

136 We report here that RANTES expression in IRF-1-null mice, primarily in macrophages, in response t

137 Thus, the increase in IRF-1 transcriptional activity observed on nanobody bind

138 y responses, and exacerbated liver injury in IRF-1-KO graft recipients.

139 thase expression in C56BL/6 mice, but not in IRF-1 knockout mice.

140 IFN-gamma mRNA was significantly reduced in IRF-1 KO graft.

141 a global type I IFN response was similar in IRF-1-deficient and -proficient macrophages during gamma

142 mutant was defective for systemic spread in IRF-1(-/-) mice, suggesting that these regulators are no

143 liver injury was significantly suppressed in IRF-1 knockout mice or in wild-type C56BL/6 mice that re

144 erial growth in macrophages and virulence in IRF-1(-/-) mice.

145 plays an important role in IFNgamma-induced IRF-1 (IFN regulatory factor 1) gene mRNA translation/pr

146 RARalpha ligand, regulates IFNgamma-induced IRF-1 by affecting multiple components of the IFNgamma s

147 ranscriptional functions of IFNgamma-induced IRF-1, increasing its nuclear localization and DNA bindi

148 acid phenethyl ester blocks L. major-induced IRF-1 and IRF-8 activation and IL-12 expression.

149 e the signaling pathways of TNFalpha-induced IRF-1 expression and IRF-1 nuclear translocation.

150 TNFalpha-induced IRF-1 expression was assessed by real-time quantitative

151 B or JNK-2 pathways reduced TNFalpha-induced IRF-1 nuclear translocation by 35% and 50%, respectively

152 This cytokine-induced, IRF-1-mediated developmental death network weakens neona

153 anges in the spleens of chronically infected IRF-1-deficient animals.

154 nst classical death receptors do not inhibit IRF-1 induced apoptosis, and no secreted ligand appears

155 ion on IFN-I-responsive macrophages inhibits IRF-1-mediated transactivation of IL-27 gene expression

156 In contrast, in testing, B cell-intrinsic IRF-1 expression promoted the MHV68-driven germinal cent

157 inase R, interferon regulatory factors (IRF) IRF-1, IRF-3, IRF-5, IRF-7, mitochondrial antiviral sign

158 Along with 43-kDa IRF-1, 4 of the 7 nuclearly located cross-reacting prote

159 etter protection compared with those lacking IRF-1 in NPC.

160 The data link IRF-1 regulatory domains to its growth inhibitory activi

161 or IFN-gamma inhibited alpha-GalCer-mediated IRF-1 upregulation.

162 s that interact with this region to modulate IRF-1 function.

163 Moreover, IRF-1 deficiency resulted in prolonged occupancy of RelA

164 s to an Hsp70-dependent depletion of nuclear IRF-1.

165 C-terminal Mf1 domain (residues 301-325) of IRF-1.

166 Correspondingly, in the absence of IRF-1, chronic gammaherpesvirus infection induced pathol

167 The antiviral actions of IRF-1 appeared to be independent of the induction of typ

168 The antiviral actions of IRF-1 resulted in decreased local inflammatory responses

169 iologic agents and that antitumor actions of IRF-1/ICSBP can be exploited therapeutically to circumve

170 strated that the transcriptional activity of IRF-1 is constrained by the Mf1 domain as nanobody bindi

171 Thus, antagonism of IRF-1 is a novel mechanism that synergizes with the note

172 ically, we demonstrate that a combination of IRF-1 and type I IFN signaling ensures host survival dur

173 Deficiency of IRF-1 signaling in graft resulted in significantly reduc

174 s to elucidate the role of the Mf1 domain of IRF-1 in orchestrating the recruitment of regulatory fac

175 r activity when the Cdk2-repressor domain of IRF-1 is mutated implicates repression as a determinant

176 e CHIP within the major disordered domain of IRF-1 led us to ask whether this region might be employe

177 A (siRNA) were used to analyze the effect of IRF-1 down-regulation on TNFalpha-induced IL-18BP expres

178 ine the extent to which antiviral effects of IRF-1 are B cell intrinsic, we generated mice with condi

179 sms responsible for the antiviral effects of IRF-1 are still poorly understood.

180 ly to contribute to the antiviral effects of IRF-1 in other virus systems.

181 and contributed to the antiviral effects of IRF-1.

182 s was associated with impaired expression of IRF-1 and proapoptotic molecules such as Fas ligand, its

183 reperfusion injury, stimulated expression of IRF-1 in an S3 proximal tubular cell line.

184 Ectopic expression of IRF-1 in epithelial cells relieved P. gingivalis-induced

185 aster, higher, and more stable expression of IRF-1 than IFNgamma alone.

186 th significant increase in the expression of IRF-1, IRF-8 and IL-27 (IL-27p28 and Ebi3).

187 overexpresses the dominant-negative form of IRF-1 (dnIRF1) specifically in oligodendrocytes.

188 nts have suggested an inhibitory function of IRF-1 against infection of alphaviruses in cell culture,

189 The new pivotal function of IRF-1 in the death of neonatal Th1 cells stems from the

190 nd assessed the early antiviral functions of IRF-1 prior to induction of adaptive B and T cell respon

191 udy indicate that the antiviral functions of IRF-1 unveiled in MHV68-infected mice with global IRF-1

192 tivate RANTES transcription independently of IRF-1 through direct physical interactions with NF-kappa

193 However, induction of IRF-1 and BTG2 mRNAs by MIS was independent of Smad1 act

194 element of the IRF-1 promoter, induction of IRF-1 and caspase-1/-3 activation.

195 events that drive the selective induction of IRF-1 and MUC4, respectively, within a single cell syste

196 omycin D completely blocked the induction of IRF-1 by the combination, suggesting regulation at the t

197 element of the IRF-1 promoter, induction of IRF-1 expression and caspase-1/-3 activation.

198 n in *HMEC-E6 cells blocked (1) induction of IRF-1, (2) caspase-1/-3 activation and (3) apoptosis.

199 tosis in *HMEC-E6 cells through induction of IRF-1.

200 n alphaT3 lens correlates with inhibition of IRF-1 and ICSBP expression.

201 based on the observation that inhibition of IRF-1 by RNA interference did not affect alpha-GalCer-in

202 Specific knockdown of IRF-1 in human primary hepatocytes gave similar results.

203 Transgenic knockout of IRF-1 ameliorated the impairment of renal function, morp

204 solated after I/R induced elevated levels of IRF-1 production by hepatocytes compared with liver pDC

205 activity as well as the transcript levels of IRF-1 target genes.

206 Conversely, the half-life of IRF-1 is increased by Hsp90 in an ATPase-dependent manne

207 In contrast, overexpression of IRF-1 greatly potentiated alpha-GalCer-induced liver inj

208 Overexpression of IRF-1 in two mouse breast cancer cell lines, C3-L5 and T

209 nd growth suppression as well as the rate of IRF-1 degradation.

210 ophoblast cells was due to a reduced rate of IRF-1 transcription relative to fibroblast cells.

211 RF-1-dependent transcription and the rate of IRF-1 turnover.

212 dies on the post-translational regulation of IRF-1 have been hampered by a lack of suitable biochemic

213 Regulation of IRF-1 will be a new therapeutic target in RA.

214 ght be employed more widely by regulators of IRF-1 function.

215 (P325A) involving the C-terminal residue of IRF-1 has been identified, which results in greater tran

216 as to determine the immunomodulatory role of IRF-1 during I/R injury following allogeneic LTx.

217 ts the underappreciated multifaceted role of IRF-1 in MHV68 infection and pathogenesis.

218 Irf1 (-/-) mice, we investigated the role of IRF-1 in modulating pathogenesis of two related arthrito

219 nt study was to directly examine the role of IRF-1 in oligodendrocyte injury and inflammatory demyeli

220 In spite of the known role of IRF-1 in stimulating type I IFN expression, induction of

221 This role of IRF-1 in the inhibition of MNV replication by IFN-gamma

222 We now show the functional significance of IRF-1 in affecting antiestrogen responsiveness in estrog

223 Overexpression or silencing of IRF-1 or miR-126 expression recapitulated the proatherog

224 mall interfering RNA-mediated suppression of IRF-1 protein expression in *HMEC-E6 cells blocked (1) i

225 Adenovirus-mediated gene transduction of IRF-1 in primary macrophages resulted in enhanced RANTES

226 e, TNFalpha induced nuclear translocation of IRF-1, with maximal translocation at 2 hours ( approxima

227 The effect on IRF-1 was also observed in DCs infected with the highly

228 Mf1 domain (amino acids 301-325) impacts on IRF-1-mediated gene repression and growth suppression as

229 o define a multiprotein binding interface on IRF-1 (Mf2 domain; amino acids 106-140) and to identify

230 The effect of TNFalpha on IRF-1 was assessed using nuclear and cytoplasmic extract

231 rthermore, stable transfection with ICSBP or IRF-1 construct inhibits lens carcinoma cell growth by u

232 s without effect on STAT1 phosphorylation or IRF-1 expression, transcription factors that are activat

233 mal tubular cells of the S3 segment produced IRF-1, which is a transcription factor that activates pr

234 alized chronically in the tail and protected IRF-1(-/-) and wild-type mice from virulent challenge, i

235 cription factor and tumor suppressor protein IRF-1 is predicted to be largely disordered outside of t

236 TNFalpha induced RASF IRF-1 expression at the messenger RNA and protein levels

237 promoter, to which endogenous or recombinant IRF-1 can physically bind in vitro and in vivo.

238 mbers and cooperation with Hsp90 to regulate IRF-1 turnover and activity.

239 We found that IL-1beta regulated IRF-1 gene expression through stimulation of p38 mitogen

240 ch is decreased in the CF airways, regulates IRF-1 in CF epithelial cells.

241 acids 301-325) that differentially regulates IRF-1 activity has been identified and this region media

242 -mediated quiescence, its upstream regulator IRF-1 was required.

243 rmined that maximal ischemic injury required IRF-1 expression by both leukocytes and radioresistant r

244 minant-negative FADD expressing cells resist IRF-1-induced apoptosis and activated downstream product

245 Further, a smaller but significant IRF-1 mRNA up-regulation was seen in WT graft nonparench

246 Surprisingly, B cell-specific IRF-1 deficiency attenuated the establishment of chronic

247 Further, we found that B cell-specific IRF-1 deficiency led to reduced levels of active tyrosin

248 ed occupancy of transcription factors STAT1, IRF-1, and associated histone acetylation at promoters a

249 Enforced expression of STAT1, IRF-1, or GATA-1 enhanced phosphorylation of STAT1, STAT

250 Thus, 16-kDa PRL inhibits the p38 MAPK/Stat1/IRF-1 pathway to attenuate iNOS/NO production in endothe

251 y the finding that Hsp90 inhibitors suppress IRF-1-dependent transcription shortly after treatment, a

252 typic abnormalities but displayed suppressed IRF-1 signaling in oligodendrocytes.

253 bserved protection was related to suppressed IRF-1 signaling and impaired expression of immune and pr

254 t received a microRNA specifically targeting IRF-1.

255 Ralpha production and suggest that targeting IRF-1 and IL-15/IL-15Ralpha may be effective in reducing

256 We further demonstrate that IRF-1 and IRF-8 obtained from L. major-infected human DC

257 Therefore, we demonstrate that IRF-1 induces a ligand-independent FADD/caspase-8-mediat

258 These observations demonstrate that IRF-1 promotes rECM-mediated apoptosis and provide evide

259 Furthermore, we demonstrate that IRF-1-induced apoptosis requires fas-associated death do

260 in immunoprecipitation, we demonstrated that IRF-1 binds to the 5' TG promoter motif, and the transcr

261 Specifically, we found that IRF-1 enforces long-term suppression of an inherently mu

262 We hypothesized that IRF-1 plays a pivotal role in liver transplant (LTx) isc

263 These results indicate that IRF-1 promotes LTx I/R injury via hepatocyte IL-15/IL-15

264 This study indicates that IRF-1 plays a critical role in the pathogenesis of EAE b

265 reased caspase-8 activities, indicating that IRF-1 mediates death ligand-induced hepatocyte death.

266 gical and virological analyses revealed that IRF-1 preferentially restricted CHIKV infection in cells

267 Our studies show that IRF-1 controlled alphavirus replication and swelling in

268 Here we show that IRF-1 expression attenuates gammaherpesvirus replication

269 These results show that IRF-1 is a key regulator of IL-18BPa expression and IL-1

270 In this study, we show that IRF-1 restricts gammaherpesvirus replication in primary

271 We show that IRF-1-mediated growth inhibition is dependent on the int

272 Our previous work has shown that IRF-1 regulates IL-27 p28 gene transcription by specific

273 Taken together, these data suggest that IRF-1 gene activation by reactive oxygen species is an e

274 tively, our in vivo experiments suggest that IRF-1 restricts CHIKV and RRV infection in stromal cells

275 Stat1 nuclear translocation to activate the IRF-1 promoter.

276 for 4 single-nucleotide polymorphisms in the IRF-1 gene.

277 te for activation of downstream genes in the IRF-1 tumor suppressor pathway using biologics.

278 mma-activating sequence (GAS) element of the IRF-1 promoter, induction of IRF-1 and caspase-1/-3 acti

279 recruitment of CBP to the GAS element of the IRF-1 promoter, induction of IRF-1 expression and caspas

280 7 to -48 in the p28 promoter overlapping the IRF-1 binding site.

281 vate IRF-1 through recruitment of CBP to the IRF-1 GAS promoter complex.

282 transcription by specifically binding to the IRF-1 response element in the p28 promoter.

283 hat cell death is further augmented when the IRF-1-infected cells are cultured with Adriamycin.

284 his domain in limiting the rate at which the IRF-1 protein is degraded.

285 en additional proteins that reacted with the IRF-1 antibody and that underwent specific competition b

286 proteins, with an epitope in common with the IRF-1 C-terminal region and IRF element DNA sequence-bin

287 erred increased TG promoter activity through IRF-1 binding.

288 with the disease-associated variant through IRF-1 binding.

289 Thus, IRF-1 in graft hepatocytes and NPC has distinct effects

290 fferential gene regulation may contribute to IRF-1 tumor suppressor activity.

291 In breast cancer cell types, IRF-1 is implicated in mediating apoptosis by both novel

292 V68 may, in a B cell-intrinsic manner, usurp IRF-1 to promote the germinal center response and expans

293 ith global IRF-1 deficiency are mediated via IRF-1 expression by non-B cell populations.IMPORTANCE Ga

294 In vitro, IRF-1 regulated both constitutive and induced expression

295 response also peaked at 2 dynes/cm(2), where IRF-1-regulated VCAM-1 expression and monocyte recruitme

296 vides an insight into the mechanism by which IRF-1 attenuates gammaherpesvirus replication in primary

297 offer an insight into the mechanism by which IRF-1 attenuates the replication of gammaherpesviruses,

298 o the two ISRE/IRF-E sites at the DRR, while IRF-1 and STAT1 are induced to bind to the two ISRE/IRF-

299 to be involved since MDA468 coincubated with IRF-1 transfected cells do not apoptose.

300 RANTES gene transcription in synergism with IRF-1.